IbeR Facilitates Stress-Resistance, Invasion and Pathogenicity of Avian Pathogenic Escherichia coli

被引:16
|
作者
Wang, Shaohui [1 ,2 ]
Bao, Yinli [2 ]
Meng, Qingmei [2 ]
Xia, Yongjie [2 ,3 ]
Zhao, Yichao [1 ]
Wang, Yang [1 ,2 ]
Tang, Fang [2 ]
ZhuGe, Xiangkai [2 ]
Yu, Shengqing [1 ]
Han, Xiangan [1 ]
Dai, Jianjun [2 ]
Lu, Chengping [2 ]
机构
[1] Chinese Acad Agr Sci, Shanghai Vet Res Inst, Shanghai 200241, Peoples R China
[2] Nanjing Agr Univ, Minist Agr, Key Lab Anim Bacteriol, Nanjing 210095, Jiangsu, Peoples R China
[3] Fudan Univ, Sch Publ Hlth, Shanghai 200032, Peoples R China
来源
PLOS ONE | 2015年 / 10卷 / 03期
基金
中国国家自然科学基金;
关键词
MICROVASCULAR ENDOTHELIAL-CELLS; BLOOD-BRAIN-BARRIER; BACTERIOPHAGE-T7; RNA-POLYMERASE; NEONATAL MENINGITIS; VIRULENCE FACTOR; AUTOTRANSPORTER ADHESIN; TYPE-1; FIMBRIAE; URINARY-TRACT; IN-VIVO; EXPRESSION;
D O I
10.1371/journal.pone.0119698
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Systemic infections by avian pathogenic Escherichia coli (APEC) are economically devastating to poultry industries worldwide. IbeR, located on genomic island GimA, was shown to serve as an RpoS-like regulator in rpoS gene mutation neonatal meningitis E. coli(NMEC) RS218. However, the role of IbeR in pathogenicity of APEC carrying active RpoS has not yet been investigated. We showed that the APEC IbeR could elicit antibodies in infected ducks, suggesting that IbeR might be involved in APEC pathogenicity. To investigate the function of IbeR in APEC pathogenesis, mutant and complementation strains were constructed and characterized. Inactivation of ibeR led to attenuated virulence and reduced invasion capacity towards DF-1 cells, brains and cerebrospinal fluid (CSF) in vitro and in vivo. Bactericidal assays demonstrated that the mutant strain had impaired resistance to environmental stress and specific pathogen-free (SPF) chicken serum. These virulence-related phenotypes were restored by genetic complementation. Quantitative real-time reverse transcription PCR revealed that IbeR controlled expression of stress-resistance genes and virulence genes, which might led to the associated virulence phenotype.
引用
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页数:16
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